| http://purl.uniprot.org/citations/10562306 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/10562306 | http://www.w3.org/2000/01/rdf-schema#comment | "It was recently shown that naturally occurring Mdr1a mutant fetuses of the CF-1 outbred mouse stock have no placental Mdr1a P-glycoprotein (P-gp) and that this absence is associated with increased sensitivity to avermectin, a teratogenic pesticide. To further define the role of placental drug-transporting P-gp in toxicological protection of the fetus, we used mice with a targeted disruption of the Mdr1a and Mdr1b genes. Mdr1a(+/-)/1b(+/-) females were mated with Mdr1a(+/-)/1b(+/-) males to obtain fetuses of 3 genotypes (Mdr1a(+/+)/1b(+/+), Mdr1a(+/-)/1b(+/-), and Mdr 1a(-/-)/1b(-/-)) in a single mother. Intravenous administration of the P-gp substrate drugs [(3)H]digoxin, [(14)C]saquinavir, or paclitaxel to pregnant dams revealed that 2.4-, 7-, or 16-fold more drug, respectively, entered the Mdr1a(-/-)/1b(-/-) fetuses than entered wild-type fetuses. Furthermore, placental P-gp activity could be completely inhibited by oral administration of the P-gp blockers PSC833 or GG918 to heterozygous mothers. Our findings imply that the placental drug-transporting P-gp is of great importance in limiting the fetal penetration of various potentially harmful or therapeutic compounds and demonstrate that this P-gp function can be abolished by pharmacological means. The latter principle could be applied clinically to improve pharmacotherapy of the unborn child."xsd:string |
| http://purl.uniprot.org/citations/10562306 | http://purl.org/dc/terms/identifier | "doi:10.1172/jci7963"xsd:string |
| http://purl.uniprot.org/citations/10562306 | http://purl.uniprot.org/core/author | "Schinkel A.H."xsd:string |
| http://purl.uniprot.org/citations/10562306 | http://purl.uniprot.org/core/author | "Smit J.W."xsd:string |
| http://purl.uniprot.org/citations/10562306 | http://purl.uniprot.org/core/author | "van Tellingen O."xsd:string |
| http://purl.uniprot.org/citations/10562306 | http://purl.uniprot.org/core/author | "Huisman M.T."xsd:string |
| http://purl.uniprot.org/citations/10562306 | http://purl.uniprot.org/core/author | "Wiltshire H.R."xsd:string |
| http://purl.uniprot.org/citations/10562306 | http://purl.uniprot.org/core/date | "1999"xsd:gYear |
| http://purl.uniprot.org/citations/10562306 | http://purl.uniprot.org/core/name | "J Clin Invest"xsd:string |
| http://purl.uniprot.org/citations/10562306 | http://purl.uniprot.org/core/pages | "1441-1447"xsd:string |
| http://purl.uniprot.org/citations/10562306 | http://purl.uniprot.org/core/title | "Absence or pharmacological blocking of placental P-glycoprotein profoundly increases fetal drug exposure."xsd:string |
| http://purl.uniprot.org/citations/10562306 | http://purl.uniprot.org/core/volume | "104"xsd:string |
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